The effects of melatonin supplementation on clinical, metabolic and genetic status in patients with Parkinson s disease: A randomized, double-blind, placebo-controlled trial

Background and Objective: Data on the effects of melatonin supplementation on clinical symptoms, metabolic profiles and gene expression related to metabolic status in Parkinson s disease (PD) are inclusive. This study was performed to evaluate the impact of melatonin supplementation on metabolic profiles and gene expression related to metabolic status in people with PD. Methods: This randomized, double-blind, placebo-controlled clinical trial was conducted among 51 patients with PD. Participants were randomly divided into two groups to intake either 10 mg melatonin (2 melatonin capsules, 5 mg each) (n=25) or placebo (n=26) once a day, 1 hour before bedtime for 12 weeks. Gene expression related to insulin and lipid metabolism was done on peripheral blood mononuclear cells (PBMCs) using RT-PCR method. Results: Melatonin supplementation significantly reduced Unified Parkinson s Disease Rating Scale (P=0.04) and Pittsburgh Sleep Quality Index (P=0.02) compared with the placebo treatment. Compared with the placebo, melatonin supplementation resulted in a significant reduction in serum high sensitivity C-reactive protein (P=0.004) and a significant elevation in plasma total antioxidant capacity (P<0.001) and total glutathione levels (P<0.001). Additionally, consuming melatonin significantly decreased serum insulin levels (P=0.01), homeostasis model of assessment-insulin resistance (P=0.007), total- (P=0.03), LDL- (P=0.04) and total-/HDL-cholesterol ratio (P=0.04) compared with the placebo. Melatonin supplementation did not affect other metabolic parameters. Conclusion: Overall, melatonin supplementation for 12 weeks to patients with PD had beneficial effects on clinical symptoms and metabolic profiles. This trial has registered in the Iranian registry of clinical trials site (ID: IRCT20170513033941N29).

Keywords:

Melatonin supplementation , Parkinson s disease , metabolic status , gene expression